Peptic Ulcer Disease (PUD)
Definition
Mucosal lesions that penetrate the muscular layer of the mucosa and form a cavity surrounded by inflammation, such a condition can be acute and chronic, as a consequence of acid-peptic activity in gastric juice.
Epidemiology
Most common cause of hospitalization for upper gastrointestinal bleeding.
It affects more than 6 million people in the United States each year.
Clinical picture
Etiology
Pathophysiology
Epithelial defense mechanisms
Gastric secretion abnormalities associated with duodenal ulcer
The presence of peptic ulcer is the result of the caustic effects of acid and pepsin in the gastrointestinal lumen, which exceed the ability of the mucosa to resist them, there are mechanisms that allow the gastric and duodenal mucosa to resist acid-peptic attack, especially through of three components:
Epithelial mechanisms
Postepithelial mechanisms
Preepithelial mechanisms
These prevent contact between epithelial cells and noxious agents in the gastrointestinal lumen. It consists of a layer of mucus and a wall of bicarbonate-rich fixed water that lines the epithelial cells and is secreted by the epithelial cells and Brunner's glands. With this, the pH of the gastroduodenal surface can be regularly maintained at neutral values, even when the pH of the lumen is below 2.
When acid and pepsin cross the preepithelial barrier, the presence of tight junctions in the apical membrane of gastric epithelial cells limits the diffusion of hydrogen ions into the mucosa.
The blood flow of the gastric and duodenal mucosa provide the energy and the necessary substrates to maintain the integrity of the epithelial cells. Transport of bicarbonate through the bloodstream prevents damage during acid secretion.
Abnormalities in gastric secretion, acid homeostasis and gastroduodenal motility
Patients with duodenal ulcer tend to be gastric acid hypersecretors, with a higher number of parietal cells, and a higher basal acid production.
Elevated pepsinogen I concentration in 50% of patients with duodenal ulcer.
Drastic decrease in acid production due to abnormalities in vagal control.
Ulcers from H. Pylori produce ammonia, which inhibits D cells and those release uncontrolled somastostatine and induce hypergastrinemia.
Most gastric ulcers occur in the gastric epithelium that does not produce acid.
Helicobacter Pylori
Chronic gastritis associated with H. pylori infection causes atrophy of the oxyntic mucosa, with subsequent development of intestinal metaplasia and extension of the non-acid producing type epithelium into the proximal stomach.
harmful reflux of material from the duodenum into the stomach may contribute to gastric ulceration in some patients.
Bile salts in duodenal juice, as well as lysolecithin, are potentially harmful agents that can cause these ulcers.
It produces most of the cases of histological gastritis and peptic ulcer disease, in addition to predisposing to the development of gastric carcinoma.
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs can damage the gastroduodenal mucosa through topical and systemic effects.
Drugs
Chemotherapy used for the treatment of cancer, has been associated with the presence of gastric and duodenal ulcers.
Crack and cocaine
Lifestyle
Zollinger-Ellison syndrome
Smoking
Alcohol
Diet
Coffe, tea, soda, spicy food, condimented foods, peppermint, and candy.
Gastric Ulcer
Duodenal ulcer
General
Complicated PUD
Dyspepsia
Gastrointestinal bleeding
Heartburn
Pain immediately after eating
No relief with the intake of antacids
Anorexia and weight loss
Relief with antiacids or food
Commonly woken up at night by pain
Pain 2-3 hours after eating
Weight gain and hyperphagia
Non intended weight loss
Gastric tube bleeding
Hemodynamic impairment with gastrointestinal bleeding
Treatment
Diagnostic
Gold Standard
Esophagogastroduodenoscopy
It can also allow biopsy for H. Pylori
Barium swallow
Urea breath test
On suspicion for H. Pylori
Confirm or rule out h pylori infection
Regular treatment
Treatment for H. Pylori
Two weeks of clarithromycin and amoxicilin
Metronidazole and clarithromycin if no improvement in 2 weeks
Histamine H2 receptor antagonists
Surgery
Proton-pump inhibitor
Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole, dexlansoprazole
Cimetidine, ranitidine, famotidine, and nizatidine.
In case of no response to treatment
Julián Juárez Padilla A01633774